In 1975 and 1976, an audio metric survey of the membership of the Audio Engineering Society (AES) suggested that some of the members are at risk for hearing loss due to the high intensity sound exposure in their employment and positions that require critical listening to sounds, frequently at high intensity levels. In 1986, a follow-up audiometric survey was conducted to reassess the hearing level of the AES members. The results of the follow-up survey are reported in "Results of the 1986 AES Audiometric Survey," Journal of The Audio Engineering Society, Vol. 36, No. 9, September 1988, pp. 686-691. So that the more casual reader may obtain a full appreciation of the environment in which the hereinbelow described present invention has been conceived, the results of the 1986 audiometric survey are summarized with reference to FIGS. 1-4.
The term "Noise Induced Hearing Loss" (NIHL) is used to refer to the general category of hearing loss produced by exposure to excessively intense sounds. Such a hearing loss can have a sudden onset as the result of a single exposure to an extremely intense sound, such as an explosion, or it can be of an insidious nature as the result of exposure to relatively low intensity sounds over a prolonged period of time.
With particular reference to FIG. 1, the loss of hearing due to high intensity or prolonged sound exposure is the result of physiological, biochemical or anatomic changes within an ear 1. Generally, the ear 1 receives ambient sound pressure waves which propagates through the ear canal 3 causing vibrating movement of the eardrum 5. The vibrating movement of the eardrum 5 is transferred to the anvil 7. The sound waves detected by the drum 5 are transferred to the cochlea 9 by the anvil 7 which induces pressure waves in the fluid filled cochlea 9. The pressure waves are transduced to electric impulses that the nervous system interprets as sound. Damage to the structures within the cochlea 9, particularly damage to the hair cells, impair the nervous system'ability to transduce the acoustic pressure waves. Hair cells that have been destroyed by noise, age, disease nor drugs are not regenerated or replaced by other cells.
Impairment to hearing may present itself as a reduced ability to discriminate between frequency or to encode rapidly changing frequency/intensity information in a signal, or as a need for greater intensity for the detection of an acoustic signal. The last of these impairment effects is an elevated auditory (hearing) threshold which is the measure used to describe hearing loss, including losses due to noise exposure. As best seen in FIG. 2, there are shown damage risk contours graphically illustrating probabilities of ear damage occurring from noise induced hearing loss. The damage risk contours are plotted against a log of frequency along the abscissa. The left hand ordinate relates to one exposure per day to full octave bands of noise. The right hand ordinate relates to 1/3 octave or narrower bands of noise. It is to be noted that damage occurs most readily in the NIHL zone of 3,000 to 6,000 Hz and at relatively low decibel levels of sound.
With further reference to FIG. 3, the loss of hearing as a result of high intensity sound exposure is again shown to occur in the NIHL frequency range. This frequency region often is the one initially affected, regardless of the sound spectral content. The susceptibility to damage of the sensory hair cells in the 3,000 to 6,000 Hz. region appears to be the result of two primary factors.
The first factor is that the hair cells responsible for the transduction of sounds in this frequency range are located in the region of the first turn of the 31/4 turn cochlea 9. Given that location, these cells are subjected to the greatest amount of stress due to shear forces caused by the travelling sound wave within the fluid filled cochlea 9. This travelling sound wave 11 is diagrammatically represented travelling through the schematic representation of the cochlea 9 in FIG. 3.
The second factor is that the ear canal 3 acts as a tube resonator and as such provides approximately 10-17 dB of gain within the frequency band of 3,000 to 5,000 Hz. The ear canal resonance (ECR) zone is shown in FIGS. 2 and 3. Also illustrated in FIG. 3 is the 3,000 to 6,000 Hz. noise induced hearing loss (NIHL) range. Although the initial noise induced hearing loss is used within the 3,000 to 6,000 Hz. region, an even broader frequency range becomes involved as the duration of the exposure to high intensity sound increases. A typical plot of audiometric threshold vs. frequency is shown in FIG. 4 which illustrates hearing loss as a result of ECR and NIHL for a thirty year old man who had been subject to substantial levels of sound over prolong periods.
In contrast to hearing loss that is a result of noise exposure, hearing loss associated with the aging process begins with high frequencies (above 4,000 Hz), so that the ear acts much like a low pass filter. As a person ages, the hearing loss spreads to include lower frequencies. However, these two sources of hearing loss are not mutually exclusive, and the combined effects of high intensity sound exposure and aging can result in a severely disabling hearing loss.
Generally, hearing impairment often goes unnoticed because hearing threshold in the predominant speech frequencies below 3,000 Hz are initially unaffected. Significant reductions in hearing can occur at or above 4,000 Hz without resulting in an obvious awareness of hearing change, so that years of noise exposure damage may elapse before a loss of hearing may be subjectively apparent. According to the National Institute of Occupational Safety and Health, impairment exists when the ability to understand speech under everyday conditions is reduced. Thus, impairment begins where the average threshold level at 1,000, 2,000 and 3,000 Hz for both ears exceed 25 dB.
As best seen in FIG. 3, the threshold of hearing is lowest in the range between approximately 800 Hz and 10 kHz. The damage risk contours of FIG. 2 show that the most damage occurs in the narrow ECR zone and NIHL zone. However, since these zones are above the normal conversational frequency levels, the detection of hearing loss of course goes unnoticed. Although early detection of hearing loss at 4000 Hz should alert an individual to the potential of further hearing loss, such detection is often not taken. Therefore, it is desireable to encourage the taking of precautions in order to minimize the contribution to hearing loss. A great need exists for an instrument which displays spectral content of ambient sound with particular emphasis on the ECR and NIHL zones, and which displays the spectral content in a way which indicates the risk to hearing loss of the intensity of sound in each spectral region. The desirability of such a device is further enhanced by the requirements imposed by both state and federal governments for noise abatement and control.
For example, 42 U.S.C. .sctn.4901, et.seq., provides for identification of major noise sources, noise emission standards for products distributed in commerce and enforcement by penalizing for prohibited acts either by criminal or civil penalties. These noise control standards not only control the overall sound intensity but may have standards directed to the frequency spectrum and duration of the sound. In the Revised Code of Washington, .sctn.70.107.010, et. seq., such standards directed to the frequency spectrum are authorized to be adopted by local authorities. Specifically, local authorities are particularly authorized to adopt standards regulating, as to time and place, the operation of individual products which produce noise above specified levels considering frequency spectrum and duration (RCW .sctn.70.107.030(b)).